General Information of the m6A Target Gene (ID: M6ATAR00753)
Target Name Interferon gamma receptor 1 (IFNGR1)
Synonyms
IFN-gamma receptor 1; IFN-gamma-R1; CDw119; Interferon gamma receptor alpha-chain; IFN-gamma-R-alpha; CD119
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Gene Name IFNGR1
Chromosomal Location 6q23.3
Family Type II cytokine receptor family
Function
Receptor subunit for interferon gamma/INFG that plays crucial roles in antimicrobial, antiviral, and antitumor responses by activating effector immune cells and enhancing antigen presentation. Associates with transmembrane accessory factor IFNGR2 to form a functional receptor. Upon ligand binding, the intracellular domain of IFNGR1 opens out to allow association of downstream signaling components JAK1 and JAK2. In turn, activated JAK1 phosphorylates IFNGR1 to form a docking site for STAT1. Subsequent phosphorylation of STAT1 leads to dimerization, translocation to the nucleus, and stimulation of target gene transcription . STAT3 can also be activated in a similar manner although activation seems weaker. IFNGR1 intracellular domain phosphorylation also provides a docking site for SOCS1 that regulates the JAK-STAT pathway by competing with STAT1 binding to IFNGR1 (By similarity).
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Gene ID 3459
Uniprot ID
INGR1_HUMAN
HGNC ID
HGNC:5439
Ensembl Gene ID
ENSG00000027697
KEGG ID
hsa:3459
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
IFNGR1 can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
Browse Regulator
Browse Disease
YTH domain-containing family protein 1 (YTHDF1) [READER]
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary Loss of YTHDF1 mediated the overexpression of Interferon gamma receptor 1 (IFNGR1) and JAK/STAT1 signaling pathway in tumor cells, which contributes to restored sensitivity to antitumor immunity. YTHDF1 is overexpressed in GC and promotes GC by inducing cell proliferation and repression of DCs-mediated antitumor immune response.
Target Regulation Down regulation
Responsed Disease Gastric cancer ICD-11: 2B72
Pathway Response JAK-STAT signaling pathway hsa04630
Cell Process Immunity
In-vitro Model YTN16 (Mouse gastric cancer cell line (YTN16))
MKN74 Gastric tubular adenocarcinoma Homo sapiens CVCL_2791
BGC-823 Gastric carcinoma Homo sapiens CVCL_3360
AGS Gastric adenocarcinoma Homo sapiens CVCL_0139
In-vivo Model MKN74 cells (5×106/tumor) expressing shNC, shYTHDF1-1, or shYTHDF1-2 were suspended in ice-cold 100 ul PBS:Matrigel gel (1:1, v/v) (Corning, USA), and subcutaneously implanted into the right dorsal flank of 4-week-old NOD.
Gastric cancer [ICD-11: 2B72]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Loss of YTHDF1 mediated the overexpression of Interferon gamma receptor 1 (IFNGR1) and JAK/STAT1 signaling pathway in tumor cells, which contributes to restored sensitivity to antitumor immunity. YTHDF1 is overexpressed in GC and promotes GC by inducing cell proliferation and repression of DCs-mediated antitumor immune response.
Responsed Disease Gastric cancer [ICD-11: 2B72]
Target Regulator YTH domain-containing family protein 1 (YTHDF1) READER
Target Regulation Down regulation
Pathway Response JAK-STAT signaling pathway hsa04630
Cell Process Immunity
In-vitro Model YTN16 (Mouse gastric cancer cell line (YTN16))
MKN74 Gastric tubular adenocarcinoma Homo sapiens CVCL_2791
BGC-823 Gastric carcinoma Homo sapiens CVCL_3360
AGS Gastric adenocarcinoma Homo sapiens CVCL_0139
In-vivo Model MKN74 cells (5×106/tumor) expressing shNC, shYTHDF1-1, or shYTHDF1-2 were suspended in ice-cold 100 ul PBS:Matrigel gel (1:1, v/v) (Corning, USA), and subcutaneously implanted into the right dorsal flank of 4-week-old NOD.
References
Ref 1 Loss of YTHDF1 in gastric tumors restores sensitivity to antitumor immunity by recruiting mature dendritic cells. J Immunother Cancer. 2022 Feb;10(2):e003663. doi: 10.1136/jitc-2021-003663.